Summary/Abstract Acquired brain injuries are major contributors to motor impairment and disability. When these injuries occur, there are few proven strategies for promoting behavioral recovery. It is clear that the deficits resulting from cortical injury are not entirely the result of the loss of the infarcted area. Rather, the disruption in the coordinated neural activity of spared regions projecting to and receiving projections from the infarcted area significantly contribute to the impairment. It is within these spared regions that significant neuroplasticity occurs. This is the basis of rehabilitative therapies ? motor learning and usage can promote reorganization by driving neural activity that manifests in new and strengthened neural connections that can compensate for or improve the motor impairment. There are current strategies to promote this neural activity, such as transcranial magnetic stimulation and transcranial direct current stimulation, but these strategies are non- specific, and have low spatial and temporal resolution. New strategies to utilize the intrinsic mechanisms of neuroplasticity for shaping how neural communication is reestablished after an injury are necessary. One mechanism for this is activity-dependent stimulation, where the intrinsic single-unit neural activity of one region drives the activity in a distant region through intracortical microstimulation. This creates an artificial communication bridge that may lead to physiological changes within and between the trigger and target regions. The objectives of this research are 1) to develop a novel approach for driving recovery after motor cortical injury by bridging disconnected regions of cortex using activity-dependent stimulation and 2) to understand neuroplasticity-related mechanistic changes resulting from the cortical stimulation with the long- term goals of creating novel strategies to promote recovery after injury related to disruption in neural communication. The central hypothesis is that, after primary motor cortical injury, many of the resulting motor deficits are due to the loss of integration of motor programs and somatosensory information within primary motor cortex, and that reestablishing premotor-sensory communication will result in behavioral improvements (Aim 1). In addition, this artificial bridging will lead to strengthened connections of the task-related neural activity between premotor and somatosensory cortex (Aim 2) which should result in the increased expression of neuroplastic markers necessary for driving novel anatomical connections (Aim 3). With this information, it will be possible to design evidence-based strategies that more effectively drive the neuroplastic mechanisms that are necessary for recovery of motor impairments after ischemic injury.